a) Development of Brn3a dependent RGC types. This year we have focused on several downstream targets of the transcription factor Brn3a, and have performed a more in depth characterization of their cellular and subcellular localization, and generated and/or employed combinatorial genetics to characterize their expression and function in RGC subtypes. In collaboration with Chai-An Mao at UT Health Science Center, we have defined the genetic interactions between Brn3a and Tbr1 in the development of specific RGC subtypes. Taking advantage of our previously published work on the partial expression overlap between Brn3a and the neurotrophin receptor Ret, we have uncovered a genetic interaction between the Neurotrophin receptor and the transcription factor, that results in a competitive mechanism between distinct RGC types during development. Manuscript is in preparation. In addition we are generating genetic tools for two further novel or recently described RGC markers that appear to be regulated by Brn3a. b) We have nearly completed our characterization of our novel Dre-dependent Brn3c-Cre conditional knock-out (manuscript in preparation) and are using our Brn3 genetic reporters to characterize further RGC subtypes, in collaboration with expert physiology and circuit groups. c) We have completed our survey of Copine expression in retina cell types, and find a high degree of expression overlap between Copines 5, 6 and 9 in Amacrines and RGCs, while Copine 4 seems to be more selective for RGCs. We are addressing the biochemical and cell biological function of these genes using yeast two hybrid, pull-down mass spectrometry and gain and loss of function paradigms in vivo and in vitro (One paper published, one in preparation). d) We have implemented a newly develop spike sorting algorithm, in collaboration with computational biologists, and have carried out a large scale survey of RGC defects in Brn3b KO retinas (manuscript in preparation). e) We have completed an in depth analysis of visually evoked defense responses in global or retina specific Brn3b KO mice, and find suprprisngly specific defects in these animals (Manuscript is under review). f) We have followed up our collaboration on RGC-32 and generated a RGC-32 conditional mouse that will allow us to tease apart the cellular role of this cell cycle regulator in tissue remodeling, and experimental models of neuronal inflammatory diseases.